Evidence for an a r Adrenoceptor Subtype Mediating Adrenergic Vasoconstriction in Wistar Normotensive and Stroke-Prone Spontaneously Hypertensive Rat Kidney

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Abstract

Summary

We wished to characterise the α1-adrenoceptor subtypes mediating renal vasoconstrictor responses in pentobarbital anaesthetised normotensive rats and stroke-prone spontaneously hypertensive rats (SPSHR). Renal nerve stimulation, close renal arterial administration of phenylephrine (PE, a mixed α1a- and α1b -adrenoceptor agonist) and methoxamine (a putative α1a -adrenoceptor agonist) resulted in frequency and dose-dependent renal vasoconstrictor responses. Both dihy-dropyridine calcium channel antagonist amlodipine (200 μg kg-1 plus 50 μg kg-1h-1 and twice this dose) and the α1a-adrenoceptor antagonist 5-methylurapidil (5 μg kg-1 plus 1.25 μg kg-1h-1 and twice this dose) suppressed renal nerve-, PE-, and methoxamine-induced vasoconstrictions by between 21 and 59% (p < 0.05–0.001) in normotensive rats and SPSHR. The α1b-adrenoceptor alkylating agonist chloroethylclonidine (5μg kg-1 plus 1.25 4mUg kg-1h-1 and twice this dose) attenuated renal nerve-mediated vasoconstrictions by 20% (p < 0.01), but not those induced by PE and methoxamine. This pattern of agonist and blocking drug interaction suggests that the renal postjunctional α1-adrenoceptors require extracellular calcium and are sensitive to 5-methylurapidil, characteristics of the α1a-adrenoceptor subtype. Moreover, a similar situation exists at the renal resistance vessels of SPSHR.

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